The following constitute principle areas of investigation in the 9 months of FY '84: 1) Demonstration that exogenous estrogen and progesterone would provide an adequate endometrium for pregnancy without ovaries by donor egg or surrogate embryo transfer. 2) The fetal thymus provides support for oogenesis. This was shown by depletion of ovarian follicles at birth after fetal thymectomy in utero. 3) Hyperstimulation of the ovaries by gonadotropins is due to a factor we have termed "gonadotropin surge inhibiting factor". It is non-steroidal, highly antigenic and rapidly cleared from circulation and receptors. 4) We have demonstrated the utility of GnRH antagonist therapy combined with gonadotropin administration to reduce individual patient response. 5) Gonadotropin therapy can induce transient hyperprolactinemia that is suppressed by bromocryptine. We suggest it may be a marker for risk of hyperstimulation syndrome. 6) We have demonstrated a practical method to distinguish in diagnosis true ovarian failure from pseudo-ovarian resistence using estrogen-progestin therapy to test suppressibility of FSH, levels in circulation and measured by RIA. If antibodies to FSH cause a deceptively high FSH, steroids will not effect FSH levels measured by RIA.